Over the last decades, the use of phylogenetic methods in the study of emerging infectious diseases has gained considerable traction in public health. Particularly, the integration of phylogenetic analyses with the understanding of the pathogen dynamics at the population level has provided powerful tools for epidemiological surveillance systems. In the same way, the development of statistical methods and theory, as well as improvement of computational efficiency for evolutionary analysis, has expanded the use of these tools for vaccine and antiviral development. Today with the Coronavirus Disease 2019 (COVID-19), this seems to be critical. In this article, we discuss how the application of phylodynamic analysis can improve the understanding of current pandemic dynamics as well as the design, selection, and evaluation of vaccine candidates and antivirals.

Infections due to Ehrlichia, Anaplasma, Dirofilaria, Mycoplasma, Babesia and Hepatozoon continue to be highly prevalent in dogs, especially in tropical and subtropical areas, where vectors of many of them are present. However, many clinical aspects of dogs have not been characterized in detail, including assessing the haematological alterations associated with them, particularly in Colombia and Latin America. A group of 100 dogs with Ehrlichia, Anaplasma, Dirofilaria, Mycoplasma, Babesia and Hepatozoon infections/exposure were assessed by blood smear serology (SNAP4DX) and PCR in Pereira, Colombia. We performed blood counts to evaluate anaemia, leukopenia/leukocytosis, neutropenia, neutrophilia, lymphopenia/lymphocytosis, monocytosis, eosinophilia, and thrombocytopenia, among other alterations. Bivariate analyses were performed on Stata^®14, with significant p < 0.05. From the total, 85% presented ≥1 infection (past or present), 66% with coinfections (≥2 pathogens) (Ehrlichia 75%), and 89% presented clinical alterations. A total of 100% showed anaemia, 70% thrombocytopenia, 61% monocytosis, and 47% neutropenia, among other alterations. Additionally, 11% presented pancytopenia and 59% bicytopenia. The median platelet count was lower in infected dogs (126,000 cells/μL) versus non-infected (221,000 cells/μL) (p = 0.003). Thrombocytopenia was higher among infected dogs (75%) versus non-infected (40%) (p = 0.006), with a 91% positive predictive value for infection. Median neutrophil count was lower in infected dogs (6591 cells/μL) versus non-infected (8804 cells/μL) (p = 0.013). Lymphocytosis occurred only among those infected (27%) (p = 0.022). Leukopenia was only observed among infected dogs (13%). Pancytopenia was only observed among infected dogs. Ehrlichiosis and other hematic infections have led to a significant burden of haematological alterations on infected dogs, including pancytopenia in a tenth of them, most with thrombocytopenia and all anemic.

Dengue virus (DENV) is a significant public health concern in Colombia, with increased transmission of DENV type 1 (DENV-1) in the departments of Risaralda and Valle del Cauca in the Central-West region of the country following a large outbreak in 2019. However, little is known about the source, genetic diversity, and evolution of circulating viruses. We obtained serum samples from individuals with acute DENV infection and analysed DENV-1 genetic diversity, phylodynamics, and phylogeography. We found that most viruses belonged to DENV-1 genotype V, and phylogenetic analysis revealed three distinct clades, each of which was most closely related to viruses from neighbouring departments of Colombia sampled over the last 5–10 years. Thus, the 2019 outbreak and subsequent DENV-1 circulation was not due to the introduction of a new lineage to the country but rather reflected local DENV-1 V dispersion and evolution. We identified amino acid positions under positive selection in structural proteins and NS1, which may have a role in immune evasion and pathogenesis. Overall, our analysis of DENV-1 V diversity, evolution, and spread within Colombia highlights the important role of genomic surveillance in understanding virus dynamics during endemic circulation and outbreaks.

Background: SARS-CoV-2 revealed important gaps in infectious disease surveillance. Molecular epidemiology can help monitoring and adapting traditional surveillance to surpass those limitations. This work aims to contrast data driven from traditional surveillance with parameters inferred from molecular epidemiology in Latin America (LATAM) Methods: We obtained epidemiological data up to 4 ^th June, 2020. We estimated Effective Reproductive Number (Re) and epidemic curves using maximum likelihood (ML). SARS-CoV-2 genomes were obtained from GISAID up to June 4 ^th 2020. We aligned sequences, generated a ML phylogenetic tree, and ran a coalescent model Birth Death SIR. Phylodynamic analysis was performed for inferring Re, number of infections and date of introduction. Findings: A total of 1,144,077 cases were reported up to 4 ^th June 2020. Countries with the largest cumulative cases were Chile, Peru and Panama. We found at least 18 different lineages circulating, with a predominance of B.1 and B.1.1. We inferred an underestimation of the daily incident cases. When contrasting observed and inferred Re, we did not find statistically significant differences except for Chile and Mexico. Temporal analysis of the introduction of SARS-CoV-2 suggested a detection lag of at least 21 days. Interpretation: Our results support that epidemiological and genomic surveillance are two complementary approaches. Even with a low number of genomes proper estimations of Re could be performed. We suggest that countries, especially developing countries, should consider to add genomic surveillance to their systems for monitoring and adapting epidemiological control of SARS-CoV-2.

Dengue virus (DENV), a member of the Flaviviridae family, is the most prevalent and medically important mosquito-borne viral pathogen. Infected cells secrete the viral non-structural protein 1 (NS1) into the bloodstream, where it can interact with endothelial cells to induce vascular leak. Host factors involved in NS1-mediated endothelial dysfunction are incompletely understood, leading us to investigate the host interactome of DENV NS1 in endothelial cells via a comparative mass spectrometry approach. We identified ephrin B1 (EFNB1) as a critical host factor in NS1-mediated endothelial barrier dysfunction and show that phosphorylation of EFNB1 is necessary for induction of barrier dysfunction. Further, we map the interface of the EFNB1-NS1 complex through biochemical and computational approaches, and we show that EFNB1-Fc-fusion proteins can act as decoys to block NS1-induced barrier dysfunction in vitro and in vivo . This study provides insights into the mechanism of flavivirus NS1-mediated endothelial barrier dysfunction and new avenues to target vascular leak.